Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000388680 | SCV000330441 | pathogenic | not provided | 2016-04-19 | criteria provided, single submitter | clinical testing | The W1740X nonsense variant in the TSC2 gene has been reported previously in association with tuberous sclerosis complex (TSC) (TSC2 LOVD). Additionally, a different nucleotide substitution, c.5220 G>A, resulting in the same nonsense variant has also been reported in association with TSC (Roberts et al., 2002). The W1740X variant is predicted to cause loss of normal protein function through protein truncation as the last 68 amino acids of the tuberin protein are lost. Therefore, the presence of W1740X is consistent with a diagnosis of TSC |
Labcorp Genetics |
RCV001852882 | SCV002236315 | pathogenic | Tuberous sclerosis 2 | 2024-10-30 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Trp1740*) in the TSC2 gene. While this is not anticipated to result in nonsense mediated decay, it is expected to disrupt the last 68 amino acid(s) of the TSC2 protein. This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with clinical features of tuberous sclerosis complex (PMID: 12136241, 31856217). ClinVar contains an entry for this variant (Variation ID: 49362). This variant disrupts a region of the TSC2 protein in which other variant(s) (p.Arg1745Glnfs*27) have been determined to be pathogenic (internal data). This suggests that this is a clinically significant region of the protein, and that variants that disrupt it are likely to be disease-causing. For these reasons, this variant has been classified as Pathogenic. |
Tuberous sclerosis database |
RCV000042622 | SCV000066416 | not provided | Tuberous sclerosis syndrome | no assertion provided | curation |